Linked Life Data

17278096

Source:http://linkedlifedata.com/resource/pubmed/id/17278096

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2007-4-2
pubmed:abstractText
Little is known about the molecular pathogenesis of neuroendocrine tumors (NET) of the gastro-entero-pancreatic (GEP) system. We analyzed genetic and epigenetic alterations as well as the CpG island methylator phenotype (CIMP). The study comprised 118 well-differentiated fore- and mid-gut GEP-NET from 71 patients. In addition to loss of heterozygosity (LOH), microsatellite instability (MSI) and the methylation status of various tumor associated genes were examined. The expression profile of p16, APC and MENIN was investigated by immunohistochemistry. None of the tumors was highly microsatellite unstable, LOH was found in 22.2%. Significant differences in promoter hypermethylation were identified in the RUNX3 and the O(6)-MGMT genes. We found a significant loss of p16 expression in insulinomas (p = 0.05) and functional NET (p = 0.01), respectively. APC was expressed less in gastrinomas (p = 0.01) and functional GEP-NET (p = 0.05) vs. nonfunctional tumors. MENIN expression was reduced in pancreatic vs. extrapancreatic NET (p = 0.008) and in insulinomas vs. nonfunctional GEP-NET (p = 0.019) and NET associated with the carcinoid syndrome (p = 0.029). Further CIMP and a Ki-67 index >10% showed a close correlation. Outcome analysis of 19 patients showed a better survival for CIMP-negative patients. The analyses identified significant genetic and epigenetic alterations in well-differentiated fore- and mid-gut NET. CIMP, similar to Ki-67, might turn out to be of prognostic relevance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
(c) 2007 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
120
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2157-64
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17278096-Adaptor Proteins, Signal Transducing, pubmed-meshheading:17278096-Adenomatous Polyposis Coli Protein, pubmed-meshheading:17278096-CpG Islands, pubmed-meshheading:17278096-Cyclin-Dependent Kinase Inhibitor p16, pubmed-meshheading:17278096-DNA Methylation, pubmed-meshheading:17278096-Gastrointestinal Neoplasms, pubmed-meshheading:17278096-Genes, APC, pubmed-meshheading:17278096-Genes, Tumor Suppressor, pubmed-meshheading:17278096-Genes, p16, pubmed-meshheading:17278096-Humans, pubmed-meshheading:17278096-Loss of Heterozygosity, pubmed-meshheading:17278096-Microsatellite Instability, pubmed-meshheading:17278096-Neuroendocrine Tumors, pubmed-meshheading:17278096-Nuclear Proteins, pubmed-meshheading:17278096-Pancreatic Neoplasms, pubmed-meshheading:17278096-Promoter Regions, Genetic, pubmed-meshheading:17278096-Proto-Oncogene Proteins
pubmed:year
2007
pubmed:articleTitle
Analysis of molecular pathways in sporadic neuroendocrine tumors of the gastro-entero-pancreatic system.
pubmed:affiliation
Department of Internal Medicine, University of Freiburg, Hugstetterstrasse 55, D-79106 Freiburg, Germany. arnold@med1.ukl-uni-freiburg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't